Alloxan (hydrate)
(Synonyms: 阿脲 一水合物) 目录号 : GC45379A toxin that selectively eliminates pancreatic β-cells
Cas No.:2244-11-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Alloxan is a toxin that selectively eliminates pancreatic β-cells in mice, rats, and certain other animals, and is used to model type 1 diabetes in humans.1 Reduction of alloxan within β-cells precedes the generation of reactive oxygen species, which in turn contribute to β-cell death.2 The dose of alloxan needed to destroy beta cells, and thus induce diabetes, depends on the animal species, route of administration, and nutritional status.2,3,4
References
1. Dunn, J.S., Duffy, E., Gilmour, M.K., et al. Further observations on the effects of alloxan on the pancreatic islets. Journal of Physiology 103(2), 233-243 (1944).
2. Szkudelski, T. The mechanism of alloxan and streptozotocin action in B cells of the rat pancreas. Physiol. Res. 50(6), 537-546 (2001).
3. Eizirik, D.L., Pipeleers, D.G., Ling, Z., et al. Major species differences between humans and rodents in the susceptibility to pancreatic β-cell injury. Proceedings of the National Academy of Sciences of the United States of America 91(20), 9253-9256 (1994).
4. Tyberg, B., Andersson, A., and Borg, L.A. Species differences in susceptibility of transplanted and cultured pancreatic islets to the β-cell toxin alloxan. General and Comparative Endocrinology 122, 238-251 (2001).
| Cas No. | 2244-11-3 | SDF | |
| 别名 | 阿脲 一水合物 | ||
| Canonical SMILES | O=C(C(C(N1)=O)=O)NC1=O.O | ||
| 分子式 | C4H2N2O4.H2O | 分子量 | 160.1 |
| 溶解度 | DMF: 5 mg/ml,DMSO: 5 mg/ml,PBS (pH 7.2): 10 mg/ml | 储存条件 | Store at -20°C,protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 6.2461 mL | 31.2305 mL | 62.461 mL |
| 5 mM | 1.2492 mL | 6.2461 mL | 12.4922 mL |
| 10 mM | 0.6246 mL | 3.123 mL | 6.2461 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Structure and Reactivity of Alloxan Monohydrate in the Liquid Phase
J Org Chem 2021 Nov 5;86(21):14553-14562.PMID:34582209DOI:10.1021/acs.joc.1c01389.
Alloxan is an important toxic glucose analogue used to induce diabetes in lab test animals. Once regarded as a "problem structure," the condensed-phase structure of anhydrous Alloxan has largely been settled, but literature inconsistencies remain for the structure of the typically employed reagent Alloxan monohydrate. Due to the criticality of structure-function relationships, we have used 1H/13C{1H} NMR, IR spectroscopy, as well as quantum mechanical (QM) calculations to probe the liquid-phase structure and reactivity of Alloxan monohydrate. In protic solvents (D2O and acetic acid-d4), hydration at the C5 carbonyl of Alloxan monohydrate occurs quantitatively to form the C5 gem-diol (5,5'-dihydroxybarbituric acid). In the aprotic solvent dimethyl sulfoxide (DMSO)-d6, there exists a mixture of the C5 gem-diol and planar tetraketo form of Alloxan monohydrate. QM calculations explain the solvent-dependent hydration reactivity, where a solvent-assisted H-atom transfer mechanism lowers the activation energy of water addition at the C5 carbonyl by ∼16 or 27 kcal/mol in water or acetic acid, respectively, compared to the unassisted hydration reaction. Prompt recrystallization of Alloxan monohydrate from boiling water does not alter the structure of the reagent. These findings probe the exact structure of Alloxan monohydrate to guide future research efforts in biological sciences and in organic synthesis.
Concentration of VEGF-A in the intraocular fluid of rats with Alloxan model of diabetes mellitus
Vestn Oftalmol 2021;137(2):12-17.PMID:33881258DOI:10.17116/oftalma202113702112.
Purpose: To study the changes in the concentration of vascular endothelial growth factor A (VEGF-A) in the intraocular fluid (IOF) of rats with Alloxan model of diabetes mellitus (DM) on insulin therapy at different time points. Material and methods: The Alloxan model of DM was simulated in 197 rats by a single intraperitoneal injection of 100 mg/kg Alloxan hydrate. The animals were divided into 3 groups 7 days after administration of Alloxan hydrate. The main group consisted of animals with Alloxan model of DM, which begain receiving single daily intraperitoneal injections of insulin at a dose of 0.9 U/kg body weight. The comparison group included animals with Alloxan model of DM, which did not receive the therapy. The control group consisted of healthy animals. The experimental animals were withdrawn from the study 1 and 4 months after the start of insulin therapy. The concentration of VEGF-A was determined in 80-90 μL of intraocular fluid collected from both eyes of each animal. Results: At 1 month, the VEGF-A concentration in the intraocular fluid in the study group (n=17; 140 [136; 210] pg/mL) was statistically significantly higher than in the comparison group (n=20; 72 [58; 86] pg/mL; pm-u<0.0004), and in the control group (n=16; 76 [62.5; 88] pg/mL; pm-u=0.0045). The comparison group did not have statistically significant differences from the control group (pm-u=0.9979). At 4 months, the VEGF-A concentration in the intraocular fluid in the study group (n=18) was 84.8 [61.1; 93.2] pg/mL, in the comparison group (n=16) - 66.4 [54.4; 73.75] pg/mL. The VEGF-A concentration in the intraocular fluid in the study group at 4 months was statistically significantly lower than in the study group at 1 month (pm-u<0.0044). Conclusion: Insulin therapy causes a statistically significant increase in the concentration of VEGF-A in the intraocular fluid of rats with Alloxan model of DM after 1 month, but after 4 months of the therapy the VEGF-A concentration falls back to the initial values.
Diabetogenic action of alloxan-like compounds: the effect of dehydrouramil hydrate hydrochloride on isolated islets of Langerhans of the rat
Diabetologia 1983 Oct;25(4):360-4.PMID:6357918DOI:10.1007/BF00253202.
Dehydrouramil hydrate hydrochloride (DHU) is an analogue of Alloxan which retains the in vivo diabetogenic activity of Alloxan but, in contrast to Alloxan, is stable in aqueous media at physiological pH. Using rat islets of Langerhans, we have studied the acute effects of DHU on B cell function. Glucose-stimulated insulin release was markedly inhibited by DHU, the concentration of DHU giving 50% inhibition (I50) was 1 mmol/l; this was lowered to 0.5 mmol/l when the islets were exposed to DHU for 5 min before elevation of glucose concentration. The basis for this change appeared to be a protective effect of glucose, since the inclusion of 3-0-methylglucose during re-incubation with DHU also attenuated the subsequent inhibition of glucose-stimulated insulin release. The inhibitory effect on glucose-stimulated insulin release of a 5-min exposure to DHU persisted throughout a subsequent 120-min period in the absence of DHU. DHU also inhibited insulin release stimulated by mannose (20 mmol/l) or by 2-ketoisocaproate (20 mmol/l) with I50 of 1 and 0.5 mmol/l respectively. Concentrations of DHU up to 1 mmol/l had no significant effect on islet glucose oxidation or ATP content; 5 mmol/l DHU did not affect the rate of glucose oxidation, but lowered the ATP content by 30% without pre-incubation and by 60% in islets pre-incubated for 5 min with DHU before addition of glucose.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetogenic action of alloxan-like compounds: cytotoxic effects of 5-hydroxy-pseudouric acid and dehydrouramil hydrate hydrochloride on rat pancreatic beta cells
Diabetologia 1984 Sep;27(3):403-6.PMID:6389244DOI:10.1007/BF00304858.
The effects on islet morphology and blood glucose concentration of intravenous administration of Alloxan to rats have been compared with those of two new diabetogenic agents, 5-hydroxy-pseudouric acid (5-HPUA) and dehydrouramil hydrate hydrochloride (DHU). Administration of Alloxan (0.35 mmol/kg) caused a classical triphasic change in blood glucose characterised by initial hyperglycaemia, subsequent hypoglycaemia and a delayed persistent hyperglycaemia. In contrast, 5-HPUA and DHU elicited persistent hyperglycaemia as early as 30 min after administration. Morphological evidence for degranulation, pyknosis, necrosis and widening of pericapillary spaces was obtained with all three agents. However, both 5-HPUA and DHU elicit considerably more rapid and extensive changes than Alloxan, with evidence for extensive pyknosis occurring as early as 15 min after administration of DHU and 5-HPUA compared with 24 h for Alloxan. The more marked potency of DHU and 5-HPUA may be at least partially attributable to the greater stability of these agents compared with Alloxan, since solutions of DHU or 5-HPUA kept for 15 min prior to administration retained full diabetogenic activity, whereas similar treatment of Alloxan solution completely abolished its diabetogenic activity. Since both 5-HPUA and DHU are potential metabolites of uric acid, their marked diabetogenic potency raises the possibility of a role for uric acid metabolites in the pathogenesis of diabetes mellitus.
Rutin ameliorates metabolic acidosis and fibrosis in Alloxan induced diabetic nephropathy and cardiomyopathy in experimental rats
Mol Cell Biochem 2020 Aug;471(1-2):41-50.PMID:32529498DOI:10.1007/s11010-020-03758-y.
Diabetic nephropathy and cardiomyopathy are two major causes of mortality among patients with diabetes mellitus (DM). Since current diabetic medications are associated with various side effects, the naturally occurring plant-derived compounds are in demand. Bioflavonoids originating from vegetables and medicinal plants have beneficial effects on diabetes by improving glycemic control, lipid metabolism, and anti-oxidant status. The present study is focused on the effect of rutin against Alloxan induced diabetic nephropathy and cardiomyopathy. Male albino Wistar rats were divided into four groups, each of six rats. Group I control rats received 0.9% saline as a single dose intraperitoneally. Group II rats were induced diabetes with a single dose of Alloxan monohydrate (150 mg/kg body weight in 0.9% saline) intraperitoneally. Group III rats received 0.28 M of NH4Cl in drinking water for 3 days for the experimental induction of metabolic acidosis. Group IV rats were injected with a single dose of Alloxan monohydrate (150 mg/kg bodyweight) and administered rutin hydrate (100 mg/kg) for a period of 4 weeks by oral gavage. Administration of rutin prevented urinary ketone body formation and decreased serum creatinine and urea levels in Alloxan induced diabetic rats. Rutin supplementation reduced the levels of serum triglycerides and cholesterol in diabetic rats. Gene expression profiling of metabolic acidosis related genes (AQP2, AQP3 and V2R) and also histopathological results demonstrated the protective effect of rutin against diabetic ketoacidodis and fibrosis. The results of the present study revealed rutin administration prevents the progression of diabetic nephropathy and cardiomyopathy through amelioration of fibrosis and metabolic acidosis.